Internal Medicine: Chronic Obstructive Pulmonary Disease - PDF

Internal Medicine Based on Kirkuk University Lectures Presented By Dr. Mohammed Alaa By Next Lecture The premature airway closure increases the volume of air retained in the lungs at the end of expiration; this is referred to as air trapping. This trapped air results in...

Internal Medicine Based on Kirkuk University Lectures Presented By Dr. Mohammed Alaa By Next Lecture The premature airway closure increases the volume of air retained in the lungs at the end of expiration; this is referred to as air trapping. This trapped air results in pulmonary hyperinflation. Therefore patients with obstructive lung disease have elevated TLC, FRC, and RV The definition of a bulla is an air-filled space of > 1 cm in diameter within the lung which has developed because of emphysematous destruction of the lung parenchyma  Chronic obstructive pulmonary disease (COPD) COPD is defined as a preventable and treatable lung disease with some significant extra-pulmonary effects that may contribute to the severity in individual patients. characterised by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities, usually caused by significant exposure to noxious particles or gases. The pulmonary component is characterised by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases.  Related diagnoses include chronic bronchitis (cough and sputum on most days for at least 3 consecutive months for at least 2 successive years) and emphysema (abnormal permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis). Extrapulmonary manifestations include impaired nutrition, weight loss and skeletal muscle dysfunction.  Epidemiology Prevalence is directly related to the prevalence of tobacco smoking and, in low- and middle-income countries, the use of biomass fuels. Current estimates suggest that 80 million people world-wide suffer from moderate to severe disease. In 2005, COPD contributed to more than 3 million deaths (5% of deaths globally), but by 2020 it is forecast to represent the third most important cause of death world-wide. The anticipated rise in morbidity and mortality from COPD will be greatest in Asian and African countries as a result of their increasing tobacco consumption.  Aetiology Cigarette smoking represents the most significant risk factor for COPD and relates to both the amount and the duration of smoking. It is unusual to develop COPD with less than 10 pack years (1 pack year = 20 cigarettes/day/year) and not all smokers develop the condition, suggesting that individual susceptibility factors are important.  Risk factors for development of COPD Exposures Tobacco smoke: accounts for 95% of cases in UK Biomass solid fuel fires: wood, animal dung, crop residues and coal lead to high levels of indoor air pollution Occupation: coal miners and those who work with cadmium Outdoor and indoor air pollution Low birth weight: may reduce maximally attained lung function in young adult life Lung growth: childhood infections or maternal smoking may affect growth of lung during childhood, resulting in a lower maximally attained lung function in adult life  Infections: recurrent infection may accelerate decline in FEV1; persistence of adenovirus in lung tissue may alter local inflammatory response predisposing to lung damage; HIV infection is associated with emphysema Low socioeconomic status Nutrition: role as independent risk factor unclear Cannabis smoking Host factors Genetic factors: α1-antiproteinase deficiency; other COPD susceptibility genes are likely to be identified Airway hyper-reactivity  presence of airflow limitation combined with premature airway closure leads to gas trapping Pathophysiology and hyperinflation, adversely affecting pulmonary and chest wall compliance. Pulmonary hyperinflation also results, COPD has both pulmonary and systemic components. The changes in pulmonary and chest wall compliance mean that collapse of intrathoracic airways during expiration is exacerbated, during exercise as the time available for expiration shortens, resulting in dynamic hyperinflation. Increased V/Q mismatch increases the dead space volume and wasted ventilation. Flattening of the diaphragmatic muscles and an increasingly horizontal alignment of the intercostal muscles place the respiratory muscles at a mechanical disadvantage.  The work of breathing is therefore markedly increased, first on exercise but, as the disease advances, at rest too. Emphysema may be classified by the pattern of the enlarged airspaces: centriacinar, panacinar and periacinar. Bullae form in some individuals. This results in impaired gas exchange and respiratory failure. The definition of a bulla is an air-filled space of > 1 cm in diameter within the lung which has developed because of emphysematous destruction of the lung parenchyma  Clinical features COPD should be suspected in any patient over the age of 40 years who presents with symptoms of chronic bronchitis and/or breathlessness. Depending on the presentation, important differential diagnoses include chronic asthma, tuberculosis, bronchiectasis and congestive cardiac failure. Cough and associated sputum production are usually the first symptoms, often referred to as a 'smoker's cough'. Haemoptysis may complicate exacerbations of COPD but should not be attributed to COPD without thorough investigation.  Breathlessness usually brings about the first presentation to medical attention. Breathlessness usually prompts presentation to a health professional. The level should be quantified for future reference, often by documenting what the patient can manage before stopping the modified Medical Research Council (MRC) dyspnoea scale may also be useful. In advanced disease, enquiry should be made as to the presence of oedema (which may be seen for the first time during an exacerbation) and morning headaches, which may suggest hypercapnia.  Physical signs are non-specific, correlate poorly with lung function, and are seldom obvious until the disease is advanced. Breath sounds are typically quiet; crackles may accompany infection but if persistent raise the possibility of bronchiectasis. Finger clubbing is not a feature of COPD and should trigger further investigation for lung cancer, bronchiectasis or fibrosis. The presence of pitting oedema should be documented but the frequently used term 'cor pulmonale' is actually a misnomer, as the right heart seldom 'fails' in COPD and the occurrence of oedema usually relates to failure of salt and water excretion by the hypoxic, hypercapnic kidney. Fatigue, anorexia and weight loss may point to the development of lung cancer or tuberculosis, but are common in patients with severe COPD.  The body mass index (BMI) is of prognostic significance and should be recorded. Two classical phenotypes have been described: 'pink puffers' and 'blue bloaters'. The former('pink puffers) are typically thin and breathless, and maintain a normal PaCO2 until the late stage of disease. The latter ('blue bloaters')develop (or tolerate) hypercapnia earlier and may develop oedema and secondary polycythaemia. In practice, these phenotypes often overlap.  Investigations Although there are no reliable radiographic signs that correlate with the severity of airflow limitation, a chest X-ray is essential to identify alternative diagnoses such as cardiac failure, other complications of smoking such as lung cancer, and the presence of bullae. A full blood count is useful to exclude anaemia or document polycythaemia, and in younger patients with predominantly basal emphysema, α1-antiproteinase should be assayed. The diagnosis requires objective demonstration of airflow obstruction by spirometry and is established when the post-bronchodilator FEV1 is less than 80% of the predicted value and accompanied by FEV1/FVC < 70%.  An FEV1/FVC < 70% with an FEV1 of 80% or more suggests the presence of mild disease, although this may be a normal finding in older patients. The severity of COPD may be defined according to the post-bronchodilator FEV1 as a percentage of the predicted value for the patient's age. A low peak flow is consistent with COPD but is non- specific, does not discriminate between obstructive and restrictive disorders, and may underestimate the severity of airflow limitation. Spirometric classification of COPD severity based on post- bronchodilator FEV1 Stage Severity FEV1 I Mild FEV1/FVC < 0.70 FEV1≥80% predicted II Moderate FEV1/FVC < 0.70 50% ≤ FEV1 < 80% predicted(50%-80%) III Severe FEV1/FVC < 0.70 30% ≤ FEV1 < 50% predicted(30%-50%) IV Very severe FEV1/FVC < 0.70 FEV1 < 30% predicted or FEV1 < 50% predicted plus chronic respiratory failure  Measurement of lung volumes provides an assessment of hyperinflation. This is generally performed using the helium dilution technique. The presence of emphysema is suggested by a low gas transfer factor. Exercise tests provide an objective assessment of exercise tolerance and a baseline on which to judge the response to bronchodilator therapy or rehabilitation programmes; they may also be valuable when assessing prognosis.  Pulse oximetry may prompt referral for a domiciliary oxygen assessment if less than 93%. HRCT is likely to play an increasing role in the assessment of COPD, as it allows the detection, characterisation and quantification of emphysema and is more sensitive than a chest X-ray at detecting bullae.  Management Smoking cessation Every attempt should be made to highlight the role of smoking in the development and progress of COPD, advising and assisting the patient toward smoking cessation. On cessation patients should be warned to expect an apparent worsening of chest symptoms and reassured that this is temporary. Cessation is difficult but highly rewarding and remains the only intervention proven to decelerate the decline in FEV1.  Smoking cessation and COPD 'Sustained smoking cessation in mild to moderate COPD is accompanied by a reduced decline in FEV1 compared to persistent smokers.'  Reducing the number of cigarettes smoked each day has little impact on the course and prognosis of COPD, but complete cessation is accompanied by an improvement in lung function and deceleration in the rate of FEV1 decline. In regions where the indoor burning of biomass fuels is important, the introduction of non-smoking cooking devices or the use of alternative fuels should be encouraged.  Pulmonary rehabilitation Exercise should be encouraged at all stages and patients should be reassured that breathlessness, whilst distressing, is not dangerous. Multidisciplinary programmes that incorporate physical training, disease education and nutritional counselling reduce symptoms, improve health status and enhance confidence.  Bronchodilator therapy is central to the management of breathlessness. The inhaled route is preferred and a number of different agents delivered by a variety of devices are available. Short-acting bronchodilators, such as the β2- agonists salbutamol and terbutaline, or the anticholinergic, ipratropium bromide, may be used for patients with mild disease.  Longer-acting bronchodilators, such as the β2- agonists salmeterol and formoterol, or the anticholinergic tiotropium bromide, are more appropriate for patients with moderate to severe disease. Significant improvements in breathlessness may be reported despite minimal changes in FEV1, probably reflecting improvements in lung emptying that reduce dynamic hyperinflation and ease the work of breathing.  Oral bronchodilator therapy may be contemplated in patients who cannot use inhaled devices efficiently. Theophylline preparations improve breathlessness and quality of life, but their use has been limited by side-effects, unpredictable metabolism and drug interactions. Bambuterol, a pro-drug of terbutaline, is used on occasion. Orally active highly selective phosphodiesterase inhibitors are currently under development.  Corticosteroids Those with frequent exacerbations and/or persistent breathlessness despite long-acting bronchodilators, may benefit from inhaled Inhaled corticosteroids (ICS) reduce the frequency and severity of exacerbations; they are currently recommended in patients with severe disease (FEV1 < 50%) who report two or more exacerbations requiring antibiotics or oral steroids per year. Regular use is associated with a small improvement in FEV1, but they do not alter the natural history of the FEV1 decline. It is more usual to prescribe a fixed combination of an ICS with a LABA. Oral corticosteroids are useful during exacerbations but maintenance therapy contributes to osteoporosis and impaired skeletal muscle function and should be avoided.  Oxygen therapy Long-term domiciliary oxygen therapy (LTOT) 'Long-term home oxygen therapy improves survival in selected patients with COPD complicated by severe hypoxaemia (arterial PaO2 less than 8.0 kPa (55 mmHg)).' Prescription of long-term oxygen therapy (LTOT) in COPD Arterial blood gases measured in clinically stable patients on optimal medical therapy on at least two occasions 3 weeks apart: 1. PaO2 < 7.3 kPa (55 mmHg) irrespective of PaCO2 and FEV1 < 1.5 L 2. PaO2 7.3-8 kPa (55-60 mmHg) plus pulmonary hypertension, peripheral oedema or nocturnal hypoxaemia 3. patient stopped smoking. Use at least 15 hours/day at 2-4 L/min to achieve a PaO2 > 8 kPa (60 mmHg) without unacceptable rise in PaCO2.  Surgical intervention Young patients in whom large bullae compress surrounding normal lung tissue, who otherwise have minimal airflow limitation and a lack of generalised emphysema, may be considered for bullectomy. Patients with predominantly upper lobe emphysema, with preserved gas transference and no evidence of pulmonary hypertension, may benefit from lung volume reduction surgery (LVRS), in which peripheral emphysematous lung tissue is resected with the aim of reducing hyperinflation and decreasing the work of breathing may lead to improvements in FEV1, lung volumes, exercise tolerance and quality of life.  Both bullectomy and LVRS can be performed thorascopically, minimising morbidity, and endoscopic techniques for lung volume reduction are also under development. Lung transplantation may benefit carefully selected patients with advanced disease but is limited by shortage of donor organs.  Other measures Patients with COPD should be offered an annual influenza vaccination and, as appropriate, pneumococcal vaccination. Obesity, poor nutrition, depression and social isolation should be identified and, if possible, improved. Mucolytic therapy such as acetylcysteine, or antioxidant agents are occasionally used but with limited evidence.  Prognosis COPD has a variable natural history but is usually progressive. The prognosis is inversely related to age and directly related to the post-bronchodilator FEV1. Additional poor prognostic indicators include weight loss and pulmonary hypertension. A recent study has suggested that a composite score (BODE index) comprising the body mass index (B), the degree of airflow obstruction (O), a measurement of dyspnoea (D) and exercise capacity (E), may assist in predicting death from respiratory and other causes. Respiratory failure, cardiac disease and lung cancer represent common modes of death. Calculation of the BODE index Points on BODE index Variable 0 1 2 3 FEV1 ≥ 65 50-64 36-49 ≤ 35 Distance ≥ 350 250-349 150-249 ≤ 149 walked in 6 min (m) MRC dyspnoea 0-1 2 3 4 scale Body mass > 21 ≤ 21 index A patient with a BODE score of 0-2 has a mortality rate of around 10% at 52 months, whereas a patient with a BODE score of 7-10 has a mortality rate of around 80% at 52 months. Acute exacerbations of COPD  Acute exacerbations of COPD Acute exacerbations of COPD are characterised by an increase in symptoms and deterioration in lung function and health status. They become more frequent as the disease progresses and are usually triggered by bacteria, viruses or a change in air quality. They may be accompanied by the development of respiratory failure and/or fluid retention and represent an important cause of death.  Many patients can be managed at home with the use of increased bronchodilator therapy, a short course of oral corticosteroids, and if appropriate, antibiotics. The presence of cyanosis, peripheral oedema or an alteration in consciousness should prompt referral to hospital. In other patients, consideration of comorbidity and social circumstances may influence decisions regarding hospital admission. Management of Acute exacerbations of COPD  Oxygen therapy In patients with an exacerbation of severe COPD, high concentrations of oxygen may cause respiratory depression and worsening acidosis. Controlled oxygen at 24% or 28% should be used with the aim of maintaining a PaO2 > 8 kPa (60 mmHg) (or an SaO2 > 90%) without worsening SaO 2 of 88%–92% acidosis. Bronchodilators Nebulised short-acting β2-agonists combined with an anticholinergic agent (e.g. salbutamol with ipratropium) should be administered.  With careful supervision, it is usually safe to drive nebulisers with oxygen, but if concern exists regarding oxygen sensitivity, nebulisers may be driven by compressed air and supplemental oxygen delivered by nasal cannula. Corticosteroids Oral prednisolone reduces symptoms and improves lung function. Currently, doses of 30 mg for 10 days are recommended but shorter courses may be acceptable. Prophylaxis against osteoporosis should be considered in patients who receive repeated courses of steroids. bisphosphonates.  Antibiotic therapy The role of bacteria in exacerbations remains controversial and there is little evidence for the routine administration of antibiotics. They are currently recommended for patients reporting an increase in sputum purulence, sputum volume or breathlessness. In most cases, simple regimens are advised, such as an aminopenicillin or a macrolide. Co-amoxiclav is only required in regions where β- lactamase-producing organisms are known to be common.  Non-invasive ventilation If, despite the above measures, the patient remains tachypnoeic and acidotic (H+ ≥ 45/pH < 7.35), then NIV should be commenced. Several studies have demonstrated its benefit. Mechanical ventilation may be contemplated in those with a reversible cause for deterioration (e.g. pneumonia), or when no prior history of respiratory failure has been noted. Non-invasive ventilation in COPD exacerbations 'Non-invasive ventilation is safe and effective in patients with an acute exacerbation of COPD complicated by mild to moderate respiratory acidosis and should be considered early in the course of respiratory failure to reduce the need for endotracheal intubation, treatment failure and mortality.‘  Additional therapy Exacerbations may be accompanied by the development of peripheral oedema; this usually responds to diuretics. There has been a vogue for using an infusion of intravenous aminophylline but evidence for benefit is limited and there are risks of inducing arrhythmias and drug interactions. The use of the respiratory stimulant doxapram has been largely superseded by the development of NIV, but it may be useful for a limited period in selected patients with a low respiratory rate.  Discharge Discharge from hospital may be planned once the patient is clinically stable on his or her usual maintenance medication. The provision of a nurse-led 'hospital at home' team providing short-term nebuliser loan improves discharge rates and provides additional support for the patient. NEXT LECTURE Onwards and Upwards CONTACT US @nextlecturesupport [email protected] www.nextlecture.org